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PLoS One. 2013 Dec 20;8(12):e82368. doi: 10.1371/journal.pone.0082368. eCollection 2013.

Clustering of the metabolic syndrome components in adolescence: role of visceral fat.

Author information

1
The Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada.
2
Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada.
3
Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
4
ÉCOBES, Recherche et transfert, Cégep de Jonquière, Jonquière, Quebec, Canada ; Department of Human Sciences, Université du Québec à Chicoutimi, Chicoutimi, Quebec, Canada.
5
Department of Psychology, Université du Québec à Chicoutimi, Chicoutimi, Quebec, Canada.
6
Community Genomic Centre, Université de Montréal, Chicoutimi, Quebec, Canada.
7
Rotman Research Institute, University of Toronto, Toronto, Ontario, Canada.

Abstract

Visceral fat (VF) promotes the development of metabolic syndrome (MetS), which emerges as early as in adolescence. The clustering of MetS components suggests shared etiologies, but these are largely unknown and may vary between males and females. Here, we investigated the latent structure of pre-clinical MetS in a community-based sample of 286 male and 312 female adolescents, assessing their abdominal adiposity (VF) directly with magnetic resonance imaging. Principal component analysis of the five MetS-defining variables (VF, blood pressure [BP], fasting serum triglycerides, HDL-cholesterol and glucose) identified two independent components in both males and females. The first component was sex-similar; it explained >30% of variance and was loaded by all but BP variables. The second component explained >20% of variance; it was loaded by BP similarly in both sexes but additional loading by metabolic variables was sex-specific. This sex-specificity was not detected in analyses that used waist circumference instead of VF. In adolescence, MetS-defining variables cluster into at least two sub-syndromes: (1) sex-similar metabolic abnormalities of obesity-induced insulin resistance and (2) sex-specific metabolic abnormalities associated with BP elevation. These results suggest that the etiology of MetS may involve more than one pathway and that some of the pathways may differ between males and females. Further, the sex-specific metabolic abnormalities associated with BP elevation suggest the need for sex-specific prevention and treatment strategies of MetS.

PMID:
24376531
PMCID:
PMC3869691
DOI:
10.1371/journal.pone.0082368
[Indexed for MEDLINE]
Free PMC Article

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